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Mapping of the Human Cysteine-Rich Intestinal Protein GeneCRIP1to the Human Chromosomal Segment 7q11.23
SHORT COMMUNICATION Mapping of the Human Cysteine-Rich Intestinal Protein Gene CRIP1 to the Human Chromosomal Segment 7q11.23 M. Garcia-Barcelo, S. K. W. Tsui, S. S. Chim, K. P. Fung, C. Y. Lee, and M. M. Y. Waye1 Department of Biochemistry, Basic Medical Sciences Building, The Chinese University of Hong Kong, Shatin, N.T., Hong Kong Received August 14, 1997; accepted November 7, 1997
We report here on the mapping of a cDNA encoding for human cysteine-rich heart protein (HCRHP), a counterpart of the murine cysteine-rich intestinal protein CRIP. By somatic cell hybrid analysis and radiation hybrid mapping, we have located the gene CRIP1 (HGMW-approved symbol) on the subcentromeric region of the q arm of human chromosome 7, flanking a deletion associated with Williams syndrome. q 1998 Academic Press
Cysteine-rich intestinal protein (CRIP) is a member of the LIM/double zinc-finger proteins belonging to the same group of proteins as cysteine-rich proteins (CSRP and CRP). These proteins differ in the number of LIM/double zinc-finger domains (4). The CRIP contains only one LIM/double zinc-finger motif, and it is thought to play a role in differentiation of murine intestinal epithelium (1). We have previously isolated the human cysteine-rich heart protein (human CRIP, Accession No. U09770) cDNA, a counterpart of the murine CRIP. Human CRIP is developmentally regulated in heart in a pattern different from that of the rat CRIP, suggesting that human CRIP is not an intestine-specific protein (20). Khoo (11) reported on the cloning and expression of another human CRIP cDNA and suggested that there are three copies of the CRIP gene in the human genome. Other recent studies demonstrated that rat CRIP expression in immune cells was regulated by a lipopolysaccharide, suggesting that CRIP may play a role in immune cell activation or differentiation or in processes associated with cellular repair (7, 10). The location of the CRIP1 gene was previously thought to be at 14q32 (1), a region harboring the IgM heavy locus and known for presenting cytogenetic abnormalities in human B- and T-cell tumors (2, 17). This assignment was based on the speculation that since CRIP1 is homologous to the rat and mouse CRIP gene, which is closely linked to the rat IgM heavy 1 To whom correspondence should be addressed. Telephone: /852-26096874. Fax: /852-26035123. E-mail: mary-waye@ cuhk.edu.hk.
chain locus and maps on mouse chromosome 12 (1), CRIP1 should therefore map to the homologous region on the human genome, which is 14q32.3. Another cysteine-rich protein (ESP1/CRP2) has been mapped to 14q32.3 (9). By means of somatic cell hybrid analysis and radiation hybrid mapping, we have mapped the CRIP1 gene to the chromosomal segment 7q11.23. For somatic cell hybrid analysis, PCR was applied to monochromosomal NIGMS Human/Rodent Somatic Cell Hybrid Mapping Panel 2 (Coriell Institute, Camden, NJ) consisting of 23 genomic DNAs from the same number of human-on-rodent somatic cell lines containing a single human chromosome each plus three control DNAs (human, Chinese hamster, and mouse) (5). Fifty nanograms of genomic DNA was used for amplification in 50 ml of PCR buffer (0.25 mM MgCl2 ; 75 mM Tris – HCl, pH 8.8; 20 mM NH4SO4 ; 0.01% Tween 20) containing 1 unit of Taq polymerase (Boehringer Mannheim), 25 mM concentrations of each of the four dNTPs, and 250 mM concentrations of each of the forward and reverse primers. Seven pairs of primer combinations were tested to obtain a human-specific band different from rodent background amplification products. Only combination of primers designed from the 5* and 3 * untranslated region yielded a human-specific band that was in all cases larger than the initially expected size, suggesting the presence of at least one intron. The specific pair of primers used to map CRIP1 was 5*TGTAGCCCGTGCCGCCCC-3 * for the forward direction and 5*-CTGCAAGCAGCCAAGGATG-3 * for the reverse direction, amplifying a region from nucleotide 13 to nucleotide 334 of the CRIP1 cDNA sequence published by Tsui et al. (20). Cycling conditions were as follows: 957C for 1 min; 30 cycles of 957C for 1 min, 577C for 1 min, 727C for 1 min 30 s followed by a final extension of 727C for 10 min. The expected size of the PCR product was 321 bp. Human genomic DNA (Human Line IMR91) and DNA from the somatic cell hybrid line NA 10791, which retains only human chromosome 7, yielded a single 600-bp band. No 600-bp PCR amplification product was detected from the rest of hybrids retaining other human GENOMICS 47, 419–422 (1998) ARTICLE NO. GE975134
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FIG. 1. PCR analysis of somatic cell hybrid DNA. Lanes are labeled 1–22, X, and Y to indicate the human chromosome retained in each hybrid. Hu, human genomic DNA; Ha, Chinese hamster DNA; Mo, mouse DNA; M, size markers of a l DNA–HindIII/fX174 DNA–HaeIII digest.
chromosomes and rodent DNA (Fig. 1). To check the identity of the PCR product, nested PCR was applied to the gel-purified PCR product using a primer combi-
nation in which the forward primer (5*-ATGCCCAAGTGTCCCAAGTG-3 *) was designed from the coding region and the reverse primer was the same primer described above. This pair of primers amplified a region from nucleotide 65 to nucleotide 334 (20). Sequencing of the 269-bp PCR product using the reverse primer from the coding region 5*-AGGTCAGCGTCTTCCCACATT-3 * (from nucleotides 182 to 162) yielded an 80-bp sequence 100% identical to that of CRIP1 cDNA (data not shown). The first pair of primers described above was used for radiation hybrid mapping (3). The radiation hybrid mapping was performed on the GeneBridge 4 whole-genome Radiation Hybrid Panel (Research Genetics, Huntsville, AL) as previously described (6). Samples were scored for the presence or absence of a 600-bp amplification product. The following data vector was generated: 0000000000 0000100110 0101010010 0011110000 0110101000 1010000100 0110000010 0100001000 1101001000 000. Using a LOD threshold of ú17, we were able to establish linkage of CRIP1 to chromosome 7. Furthermore, the data placed the CRIP1 gene at 7.47 cR (LODú3) below framework marker D7S669, which maps 415.77 cR from the top of the
FIG. 2. Portion of chromosome 7 q with CRIP1 placed on the radiation hybrid framework map. The numbers on the chromosome indicate the distance from the nearest marker shown on the right. 1 cR represents 1% frequency of breakage between the markers. Data obtained from Whitehead Institute Center for Genome Research are available at: http//www-genome.wi.mit.edu/ftp/pub/software/ rhmapper.
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chromosome 7 linkage group, locating CRIP1 at about 419 cR from the top telomere of the short arm. The precise order of the markers is shown in Fig. 2. We found some discrepancies in the relative order of D7S669 and D7S675: according to the Whitehead Institute/MIT Center for Genome Research, D7S669 (415.77 cR) occupies a more centromeric locus than D7S675 (423.89 cR), whereas Ge´ ne´ thon places D7S675 in the centromeric position. Nevertheless, D7S669 and D7S675 are two well-established markers flanking the telomeric breakpoint of the 7q11.23 deletion that is associated with Williams – Beuren syndrome (WS) (14, 16, 18). WS is a developmental genetic disorder with variable phenotypic expression including cardiovascular diseases with autosomal dominant inheritance (12, 13). The variability in the phenotype could be due to differences in the size of the deletion, which is likely to be greater than 950 kb (14, 15). Further understanding of the genes close to WS region could help us to define the mechanisms underlying other WS features. The 7q11.23 region contains a hot spot for multiple breakpoints, indicative of a general regional instability (18). Sequences within this region in the vicinity of the breakpoints are duplicated and clustered within a relatively small chromosomal interval. This structure provides a hypothetical mechanism for aberrant recombination or replication events, either by unequal crossover or by intrachromosomal rearrangements (16). This region has been involved in variants of the Philadelphia translocations in chronic myeloid leukemia patients (12) and in several cases of acute lymphoblastic leukemia (21). The 7q11.2 region also contains another zinc-finger protein gene, ZNF138, described as a putative candidate gene for both developmental and malignant disorders (19). Initially, CRIP1 was thought to map to 14q32, another hot spot for translocation region (8), near the CRP2 gene. Our results demonstrate that both genes are located on regions of great instability, which could explain a common origin followed by an evolutionary divergence due to cytogenetic rearrangements. A direct and inverted reciprocal chromosome insertion between 7q11.23 and 14q32.2 has been described in a woman with recurrent miscarriages (23). CRIP1 codes for a single LIM domain protein and it might represent a precursor to other genes encoding multiple LIM domain proteins (22).
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ACKNOWLEDGMENTS This study was supported by Hong Kong RGC Earmarked Grant CUHK 205/96M and the Ho Sing-Hang Education Endowment Fund. M. Garcia-Barcelo was supported by a postdoctoral fellowship from CUHK and the Ho Sing-Hang Education Endowment Fund.
REFERENCES
GENO 5134
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17. 18.
1. Birkenmeir, E. H., and Gordon, J. I. (1986). Developmental regulation of a gene that encodes a cysteine-rich intestinal protein
AID
16.
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421
and maps near the murine immunoglobulin heavy chain locus. Proc. Natl. Acad. Sci. USA 88: 2516–2520. Boehm, T., and Rabbitts, T. H. (1989). A chromosomal basis of lymphoid malignacy in man. Eur. J. Biochem. 185: 1–17. Cox, R. D., Burmeister, M., Price, E. R., Kim, S., and Myers, R. M. (1990). Radiation hybrid mapping: A somatic cell genetic method for constructing high-resolution maps of mammalian chromosomes. Science 250: 245–250. Crawford, A. W., Pino, J. D., and Beckerle, M. C. (1994). Biochemical and molecular characterization of the chicken cysteine-rich protein, a developmentally regulated LIM-domain protein that is associated with the actin cytoskeleton. J. Cell Biol. 124: 117–127. Drwinga, H. L., Toji, L. H., Kim, C. H., Greene, A. E., and Mulivor, R. A. (1993). NIGMS human/rodent somatic cell hybrid mapping panels 1 and 2. Genomics 16: 311–314. Garcia-Barcelo, M., Law, P. T. W., Tsui, S. K. W., Fung, K. P., Lee C. Y., and Waye, M.M.Y. (1997). Mapping of the human ribosomal large subunit protein gene RPL29 to human chromosome 3q29–qter. Genomics, in press. Hallquist N. A., Khoo, C., and Cousins, R. J. (1996). Lipopolysaccharide regulates cysteine-rich intestinal protein, a zincfinger protein in immune cells and plasma. J. Leukocyte Biol. 59: 172–177. Hofler, M. H., Smith, S., Nakamura, Y., Teshima, I., White, R., and Cox, D. W. (1990). Physical mapping of probes with 14q32, a subtelomeric region showing a high recombination frequency. Genomics 6: 33–38. Karim, M. A., Ohta, K., Egashira, M., Jinno Y., Niikawa, N., Matsuda, I., and Indo, Y. (1996). Human ESP1/CRP2, a member of the LIM domain protein family: Characterization of the cDNA and assignment of the gene locus to chromosome 14q32.3. Genomics 31: 167–176. Khoo, C., Hallquist, N. A., Samuelson, D. A., and Cousins, R. J. (1996). Differential expression of cysteine-rich intestinal protein in liver and intestine in CC14-induced inflammation. Am. J. Physiol. 270: 613–618. Khoo, C. (1997). Human cysteine-rich intestinal protein: cDNA cloning and expression of recombinant protein and identification in human peripheral blood mononuclear cells. Protein Expr. Purif. 9: 379–387. Morris, C. A., Demsey, S. A., Leonard, C. O., Dilts, C., and Blackburn, B. L. (1988). The natural history of Williams syndrome: Physical characteristics. J. Pediatr. 113: 318–326. Morris, C. A., Thomas, I. T., and Greenberg, F. (1993). Williams syndrome: Autosomal dominant inheritance. Am. J. Med. Genet. 47: 478–481. Osborne, L. R., Martindale, D., Scherer, S. W., Shi, X. M., Huizenga, J., Heng, H. H. Q., Costa, T., Pober, B., Lew, L., Brinkman, J., Rommens, J., Koop, B., and Tsui, L.C. (1996). Identification of genes from a 500-kb region at 7q11.23 that is commonly deleted in Williams syndrome patients. Genomics 36: 328–336. Osborne, L. R., Soder, S., Shi, X. M., Pober, B., Costa, T., Scherer, S. W., and L. C. Tsui. (1997). Hemizygous deletion of the Syntaxin 1A gene in individuals with Williams syndrome. Am. J. Hum. Genet. 61: 449–452. Perez-Jurado, L. A., Peoples, R., Kaplan, P., and Hamel, B. C. J. (1996). Molecular definition of the chromosome 7 deletion in Williams syndrome and parent-of origin effects on growth. Am. J. Hum. Genet. 59: 781–792. Rabbitts, T. H., (1994). Chromosomal translocations in human cancer. Nature 372: 143–149. Robinson, W. P., Waslynka, J., Bernasconi, F., Wang, M., Clark, S., Kotzot, D., and Schinzel, A. (1996). Delineation of 7q11.2 deletions associated with Williams–Beuren syndrome and
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SHORT COMMUNICATION mapping of a repetitive sequence to within and to either side of the common deletion. Genomics 34: 17–23.
19. Tommerup, N., and Vissing, H. (1995). Isolation and fine mapping of 16 novel zinc finger-encoding cDNAs identify putative candidate genes for developmental and malignant disorders. Genomics 27: 259–264. 20. Tsui, S. K. W., Yam, N. Y. H., Lee, C. Y., and Waye, M. M. Y. (1994). Isolation and characterization of a cDNA that codes for a LIM-containing protein which is developmentally regulated in heart. Biochem. Biophys. Res. Commun. 205: 497–505. 21. Uckum, F. M., Gajl-Peczalska, K. J., Provisor, A. J., and
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Heerema, N. A. (1989). Immunophenotype-karyotype associations in human acute lymphoblastic leukemia. Blood 73: 271– 280. 22. Wang, X., Ray, K., Szpirer, J., Levan, G., Liebhaber, S. A., and Cooke, N. E. (1992). Analysis of the human cysteine-rich protein gene (CSRP), assignment to chromosome 1q24–1q32, and identification of an associated MSPI polymorphism. Genomics 14: 391–397. 23. Wang, Y. T., Bajalica, S., Han, F. Y., Wang, Z. C., Bui, T. H., and Xie, Y. G. (1994). Direct and inverted reciprocal chromosome insertions between chromosomes 7 and 14 in a woman with recurrent miscarriages. Am. J. Med. Genet. 52: 349–351.
gnmxas
We report here on the mapping of a cDNA encoding for human cysteine-rich heart protein (HCRHP), a counterpart of the murine cysteine-rich intestinal protein CRIP. By somatic cell hybrid analysis and radiation hybrid mapping, we have located the gene CRIP1 (HGMW-approved symbol) on the subcentromeric region of the q arm of human chromosome 7, flanking a deletion associated with Williams syndrome. q 1998 Academic Press
Cysteine-rich intestinal protein (CRIP) is a member of the LIM/double zinc-finger proteins belonging to the same group of proteins as cysteine-rich proteins (CSRP and CRP). These proteins differ in the number of LIM/double zinc-finger domains (4). The CRIP contains only one LIM/double zinc-finger motif, and it is thought to play a role in differentiation of murine intestinal epithelium (1). We have previously isolated the human cysteine-rich heart protein (human CRIP, Accession No. U09770) cDNA, a counterpart of the murine CRIP. Human CRIP is developmentally regulated in heart in a pattern different from that of the rat CRIP, suggesting that human CRIP is not an intestine-specific protein (20). Khoo (11) reported on the cloning and expression of another human CRIP cDNA and suggested that there are three copies of the CRIP gene in the human genome. Other recent studies demonstrated that rat CRIP expression in immune cells was regulated by a lipopolysaccharide, suggesting that CRIP may play a role in immune cell activation or differentiation or in processes associated with cellular repair (7, 10). The location of the CRIP1 gene was previously thought to be at 14q32 (1), a region harboring the IgM heavy locus and known for presenting cytogenetic abnormalities in human B- and T-cell tumors (2, 17). This assignment was based on the speculation that since CRIP1 is homologous to the rat and mouse CRIP gene, which is closely linked to the rat IgM heavy 1 To whom correspondence should be addressed. Telephone: /852-26096874. Fax: /852-26035123. E-mail: mary-waye@ cuhk.edu.hk.
chain locus and maps on mouse chromosome 12 (1), CRIP1 should therefore map to the homologous region on the human genome, which is 14q32.3. Another cysteine-rich protein (ESP1/CRP2) has been mapped to 14q32.3 (9). By means of somatic cell hybrid analysis and radiation hybrid mapping, we have mapped the CRIP1 gene to the chromosomal segment 7q11.23. For somatic cell hybrid analysis, PCR was applied to monochromosomal NIGMS Human/Rodent Somatic Cell Hybrid Mapping Panel 2 (Coriell Institute, Camden, NJ) consisting of 23 genomic DNAs from the same number of human-on-rodent somatic cell lines containing a single human chromosome each plus three control DNAs (human, Chinese hamster, and mouse) (5). Fifty nanograms of genomic DNA was used for amplification in 50 ml of PCR buffer (0.25 mM MgCl2 ; 75 mM Tris – HCl, pH 8.8; 20 mM NH4SO4 ; 0.01% Tween 20) containing 1 unit of Taq polymerase (Boehringer Mannheim), 25 mM concentrations of each of the four dNTPs, and 250 mM concentrations of each of the forward and reverse primers. Seven pairs of primer combinations were tested to obtain a human-specific band different from rodent background amplification products. Only combination of primers designed from the 5* and 3 * untranslated region yielded a human-specific band that was in all cases larger than the initially expected size, suggesting the presence of at least one intron. The specific pair of primers used to map CRIP1 was 5*TGTAGCCCGTGCCGCCCC-3 * for the forward direction and 5*-CTGCAAGCAGCCAAGGATG-3 * for the reverse direction, amplifying a region from nucleotide 13 to nucleotide 334 of the CRIP1 cDNA sequence published by Tsui et al. (20). Cycling conditions were as follows: 957C for 1 min; 30 cycles of 957C for 1 min, 577C for 1 min, 727C for 1 min 30 s followed by a final extension of 727C for 10 min. The expected size of the PCR product was 321 bp. Human genomic DNA (Human Line IMR91) and DNA from the somatic cell hybrid line NA 10791, which retains only human chromosome 7, yielded a single 600-bp band. No 600-bp PCR amplification product was detected from the rest of hybrids retaining other human GENOMICS 47, 419–422 (1998) ARTICLE NO. GE975134
419
0888-7543/98 $25.00 Copyright q 1998 by Academic Press All rights of reproduction in any form reserved.
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FIG. 1. PCR analysis of somatic cell hybrid DNA. Lanes are labeled 1–22, X, and Y to indicate the human chromosome retained in each hybrid. Hu, human genomic DNA; Ha, Chinese hamster DNA; Mo, mouse DNA; M, size markers of a l DNA–HindIII/fX174 DNA–HaeIII digest.
chromosomes and rodent DNA (Fig. 1). To check the identity of the PCR product, nested PCR was applied to the gel-purified PCR product using a primer combi-
nation in which the forward primer (5*-ATGCCCAAGTGTCCCAAGTG-3 *) was designed from the coding region and the reverse primer was the same primer described above. This pair of primers amplified a region from nucleotide 65 to nucleotide 334 (20). Sequencing of the 269-bp PCR product using the reverse primer from the coding region 5*-AGGTCAGCGTCTTCCCACATT-3 * (from nucleotides 182 to 162) yielded an 80-bp sequence 100% identical to that of CRIP1 cDNA (data not shown). The first pair of primers described above was used for radiation hybrid mapping (3). The radiation hybrid mapping was performed on the GeneBridge 4 whole-genome Radiation Hybrid Panel (Research Genetics, Huntsville, AL) as previously described (6). Samples were scored for the presence or absence of a 600-bp amplification product. The following data vector was generated: 0000000000 0000100110 0101010010 0011110000 0110101000 1010000100 0110000010 0100001000 1101001000 000. Using a LOD threshold of ú17, we were able to establish linkage of CRIP1 to chromosome 7. Furthermore, the data placed the CRIP1 gene at 7.47 cR (LODú3) below framework marker D7S669, which maps 415.77 cR from the top of the
FIG. 2. Portion of chromosome 7 q with CRIP1 placed on the radiation hybrid framework map. The numbers on the chromosome indicate the distance from the nearest marker shown on the right. 1 cR represents 1% frequency of breakage between the markers. Data obtained from Whitehead Institute Center for Genome Research are available at: http//www-genome.wi.mit.edu/ftp/pub/software/ rhmapper.
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chromosome 7 linkage group, locating CRIP1 at about 419 cR from the top telomere of the short arm. The precise order of the markers is shown in Fig. 2. We found some discrepancies in the relative order of D7S669 and D7S675: according to the Whitehead Institute/MIT Center for Genome Research, D7S669 (415.77 cR) occupies a more centromeric locus than D7S675 (423.89 cR), whereas Ge´ ne´ thon places D7S675 in the centromeric position. Nevertheless, D7S669 and D7S675 are two well-established markers flanking the telomeric breakpoint of the 7q11.23 deletion that is associated with Williams – Beuren syndrome (WS) (14, 16, 18). WS is a developmental genetic disorder with variable phenotypic expression including cardiovascular diseases with autosomal dominant inheritance (12, 13). The variability in the phenotype could be due to differences in the size of the deletion, which is likely to be greater than 950 kb (14, 15). Further understanding of the genes close to WS region could help us to define the mechanisms underlying other WS features. The 7q11.23 region contains a hot spot for multiple breakpoints, indicative of a general regional instability (18). Sequences within this region in the vicinity of the breakpoints are duplicated and clustered within a relatively small chromosomal interval. This structure provides a hypothetical mechanism for aberrant recombination or replication events, either by unequal crossover or by intrachromosomal rearrangements (16). This region has been involved in variants of the Philadelphia translocations in chronic myeloid leukemia patients (12) and in several cases of acute lymphoblastic leukemia (21). The 7q11.2 region also contains another zinc-finger protein gene, ZNF138, described as a putative candidate gene for both developmental and malignant disorders (19). Initially, CRIP1 was thought to map to 14q32, another hot spot for translocation region (8), near the CRP2 gene. Our results demonstrate that both genes are located on regions of great instability, which could explain a common origin followed by an evolutionary divergence due to cytogenetic rearrangements. A direct and inverted reciprocal chromosome insertion between 7q11.23 and 14q32.2 has been described in a woman with recurrent miscarriages (23). CRIP1 codes for a single LIM domain protein and it might represent a precursor to other genes encoding multiple LIM domain proteins (22).
2. 3.
4.
5.
6.
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ACKNOWLEDGMENTS This study was supported by Hong Kong RGC Earmarked Grant CUHK 205/96M and the Ho Sing-Hang Education Endowment Fund. M. Garcia-Barcelo was supported by a postdoctoral fellowship from CUHK and the Ho Sing-Hang Education Endowment Fund.
REFERENCES
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17. 18.
1. Birkenmeir, E. H., and Gordon, J. I. (1986). Developmental regulation of a gene that encodes a cysteine-rich intestinal protein
AID
16.
01-15-98 12:23:49
421
and maps near the murine immunoglobulin heavy chain locus. Proc. Natl. Acad. Sci. USA 88: 2516–2520. Boehm, T., and Rabbitts, T. H. (1989). A chromosomal basis of lymphoid malignacy in man. Eur. J. Biochem. 185: 1–17. Cox, R. D., Burmeister, M., Price, E. R., Kim, S., and Myers, R. M. (1990). Radiation hybrid mapping: A somatic cell genetic method for constructing high-resolution maps of mammalian chromosomes. Science 250: 245–250. Crawford, A. W., Pino, J. D., and Beckerle, M. C. (1994). Biochemical and molecular characterization of the chicken cysteine-rich protein, a developmentally regulated LIM-domain protein that is associated with the actin cytoskeleton. J. Cell Biol. 124: 117–127. Drwinga, H. L., Toji, L. H., Kim, C. H., Greene, A. E., and Mulivor, R. A. (1993). NIGMS human/rodent somatic cell hybrid mapping panels 1 and 2. Genomics 16: 311–314. Garcia-Barcelo, M., Law, P. T. W., Tsui, S. K. W., Fung, K. P., Lee C. Y., and Waye, M.M.Y. (1997). Mapping of the human ribosomal large subunit protein gene RPL29 to human chromosome 3q29–qter. Genomics, in press. Hallquist N. A., Khoo, C., and Cousins, R. J. (1996). Lipopolysaccharide regulates cysteine-rich intestinal protein, a zincfinger protein in immune cells and plasma. J. Leukocyte Biol. 59: 172–177. Hofler, M. H., Smith, S., Nakamura, Y., Teshima, I., White, R., and Cox, D. W. (1990). Physical mapping of probes with 14q32, a subtelomeric region showing a high recombination frequency. Genomics 6: 33–38. Karim, M. A., Ohta, K., Egashira, M., Jinno Y., Niikawa, N., Matsuda, I., and Indo, Y. (1996). Human ESP1/CRP2, a member of the LIM domain protein family: Characterization of the cDNA and assignment of the gene locus to chromosome 14q32.3. Genomics 31: 167–176. Khoo, C., Hallquist, N. A., Samuelson, D. A., and Cousins, R. J. (1996). Differential expression of cysteine-rich intestinal protein in liver and intestine in CC14-induced inflammation. Am. J. Physiol. 270: 613–618. Khoo, C. (1997). Human cysteine-rich intestinal protein: cDNA cloning and expression of recombinant protein and identification in human peripheral blood mononuclear cells. Protein Expr. Purif. 9: 379–387. Morris, C. A., Demsey, S. A., Leonard, C. O., Dilts, C., and Blackburn, B. L. (1988). The natural history of Williams syndrome: Physical characteristics. J. Pediatr. 113: 318–326. Morris, C. A., Thomas, I. T., and Greenberg, F. (1993). Williams syndrome: Autosomal dominant inheritance. Am. J. Med. Genet. 47: 478–481. Osborne, L. R., Martindale, D., Scherer, S. W., Shi, X. M., Huizenga, J., Heng, H. H. Q., Costa, T., Pober, B., Lew, L., Brinkman, J., Rommens, J., Koop, B., and Tsui, L.C. (1996). Identification of genes from a 500-kb region at 7q11.23 that is commonly deleted in Williams syndrome patients. Genomics 36: 328–336. Osborne, L. R., Soder, S., Shi, X. M., Pober, B., Costa, T., Scherer, S. W., and L. C. Tsui. (1997). Hemizygous deletion of the Syntaxin 1A gene in individuals with Williams syndrome. Am. J. Hum. Genet. 61: 449–452. Perez-Jurado, L. A., Peoples, R., Kaplan, P., and Hamel, B. C. J. (1996). Molecular definition of the chromosome 7 deletion in Williams syndrome and parent-of origin effects on growth. Am. J. Hum. Genet. 59: 781–792. Rabbitts, T. H., (1994). Chromosomal translocations in human cancer. Nature 372: 143–149. Robinson, W. P., Waslynka, J., Bernasconi, F., Wang, M., Clark, S., Kotzot, D., and Schinzel, A. (1996). Delineation of 7q11.2 deletions associated with Williams–Beuren syndrome and
gnmxas
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SHORT COMMUNICATION mapping of a repetitive sequence to within and to either side of the common deletion. Genomics 34: 17–23.
19. Tommerup, N., and Vissing, H. (1995). Isolation and fine mapping of 16 novel zinc finger-encoding cDNAs identify putative candidate genes for developmental and malignant disorders. Genomics 27: 259–264. 20. Tsui, S. K. W., Yam, N. Y. H., Lee, C. Y., and Waye, M. M. Y. (1994). Isolation and characterization of a cDNA that codes for a LIM-containing protein which is developmentally regulated in heart. Biochem. Biophys. Res. Commun. 205: 497–505. 21. Uckum, F. M., Gajl-Peczalska, K. J., Provisor, A. J., and
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GENO 5134
/
6r58$$$421
01-15-98 12:23:49
Heerema, N. A. (1989). Immunophenotype-karyotype associations in human acute lymphoblastic leukemia. Blood 73: 271– 280. 22. Wang, X., Ray, K., Szpirer, J., Levan, G., Liebhaber, S. A., and Cooke, N. E. (1992). Analysis of the human cysteine-rich protein gene (CSRP), assignment to chromosome 1q24–1q32, and identification of an associated MSPI polymorphism. Genomics 14: 391–397. 23. Wang, Y. T., Bajalica, S., Han, F. Y., Wang, Z. C., Bui, T. H., and Xie, Y. G. (1994). Direct and inverted reciprocal chromosome insertions between chromosomes 7 and 14 in a woman with recurrent miscarriages. Am. J. Med. Genet. 52: 349–351.
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